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Molecular Mechanisms and Therapeutic Approaches in Fibrosis and Tissue Remodeling
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Molecular Mechanisms and Therapeutic Approaches in Fibrosis and Tissue Remodeling

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 31 March 2027 | Viewed by 1067

Editors

Dr. Pulin Che

E-Mail Website
Guest Editor
Department of Anesthesiology and Perioperative Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA
Interests: lung fibrosis; tissue injury and remodeling
Special Issues, Collections and Topics in MDPI journals
Dr. Huachun Cui

E-Mail Website
Guest Editor
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: inflammation; non-coding RNAs; cellular metabolism in lung injury and fibrosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fibrosis and tissue remodeling are hallmarks of numerous chronic and progressive diseases affecting the lung, liver, kidney, heart, and other organs. Advances in molecular biology, omics technologies, and preclinical models have significantly expanded our understanding of the signaling networks, cellular crosstalk, and metabolic changes underlying fibrotic pathogenesis. Despite this progress, effective therapies remain limited, and a deeper mechanistic insight is crucial to guide the development of novel interventions. This Special Issue, ‘Molecular Mechanisms and Therapeutic Approaches in Fibrosis and Tissue Remodeling’, invites original research articles, reviews, and perspectives that explore fundamental pathways, emerging biomarkers, and innovative therapeutic strategies. Our aim is to foster interdisciplinary discussion and accelerate translation from bench to bedside in the fight against fibrotic diseases.

Dr. Pulin Che
Dr. Huachun Cui
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • fibrosis
  • tissue remodeling
  • biomarkers
  • molecular pathways
  • translational medicine
  • therapeutic strategies

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Published Papers (3 papers)

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Research

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24 pages, 2790 KB  
Article
Shared and Disease-Preferential Matrisome Programs in Fibrosing Interstitial Lung Disease: Evidence from Cross-Cohort and Within-Cohort Analysis
by Xu Zhang, Yuan Wang and Pulin Che
Curr. Issues Mol. Biol. 2026, 48(9), 951; https://doi.org/10.3390/cimb48090951 - 17 Sep 2026
Abstract
Idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis (HP), and systemic sclerosis-associated interstitial lung disease (SSc-ILD) share the same structural outcome: extracellular matrix (ECM) deposition. Whether this shared endpoint reflects shared or distinct molecular programs remains unresolved. Differential expression results from four GEO datasets representing [...] Read more.
Idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis (HP), and systemic sclerosis-associated interstitial lung disease (SSc-ILD) share the same structural outcome: extracellular matrix (ECM) deposition. Whether this shared endpoint reflects shared or distinct molecular programs remains unresolved. Differential expression results from four GEO datasets representing IPF, HP, non-IPF ILD, and SSc-ILD were intersected with the 1027-gene human matrisome masterlist and classified by threshold-defined disease preference. All four diseases shared a 21-gene upregulated matrisome core, and the matrisome fraction rose with cross-disease sharing, from 4.3% of single-disease upregulated genes to 45.7% of genes upregulated in all four (significant Cochran–Armitage trend), and the enrichment persisted when any single cohort was removed. Apparent disease preference was largely attributable to unequal statistical power: of 29 genes measurable in all four datasets, 24 showed a concordant sub-threshold effect in at least one comparator disease. Category composition of the threshold-defined signatures did not differ significantly between diseases, and the exploratory pathway panel is reported within diseases only, because significance scales with cohort size. In a within-cohort comparison of IPF with chronic HP in GSE150910, with platform, cohort, and control population held constant, matrisome genes were over-represented among the 2732 genes separating the two diseases, and 205 matrisome genes distinguished them. Fibrosing ILDs share a cross-cohort ECM core, and the apparent disease preference of the remaining signatures largely reflects differences in statistical power between cohorts. Disease-preferential matrisome expression is nonetheless detectable when disease and study are not confounded, so the limitation lies in threshold-based cross-study intersection rather than in the matrisome compartment itself. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Approaches in Fibrosis and Tissue Remodeling)
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22 pages, 27096 KB  
Article
Bazedoxifene Attenuates Isoproterenol-Induced Cardiac Fibroblast Activation and Fibrotic Phenotype via Modulation of the IL-6/STAT3 Signaling Axis
by Xiangyun Chen, Taomei Yang, Xiaofang Tang, Mengyue Guo, Lixue He and Yaofeng Li
Curr. Issues Mol. Biol. 2026, 48(9), 879; https://doi.org/10.3390/cimb48090879 - 29 Aug 2026
Viewed by 187
Abstract
Bazedoxifene (BAZ), a selective estrogen receptor modulator, has recently been demonstrated to inhibit the IL-6/STAT3 signaling pathway; however, its direct effects on cardiac fibroblasts and the underlying mechanisms remain unclear. Isoproterenol (ISO)-stimulated Sprague–Dawley neonatal rat cardiac fibroblasts (CFs) were employed as an in [...] Read more.
Bazedoxifene (BAZ), a selective estrogen receptor modulator, has recently been demonstrated to inhibit the IL-6/STAT3 signaling pathway; however, its direct effects on cardiac fibroblasts and the underlying mechanisms remain unclear. Isoproterenol (ISO)-stimulated Sprague–Dawley neonatal rat cardiac fibroblasts (CFs) were employed as an in vitro model. CCK-8 assay, flow cytometry, Transwell migration assay, ELISA, qRT-PCR, and Western blot were applied to evaluate the effects of BAZ on CF activation, proliferation, migration, and collagen synthesis. Additionally, IL-6 overexpression via lentivirus (Lv-IL-6) was used to assess mediation by IL-6/STAT3 signaling. BAZ (5 μmol/L) significantly inhibited ISO-induced CF proliferation by inducing G0/G1 cell-cycle arrest; migration and upregulation of α-SMA and Collagen I/III were reduced; IL-6, TGF-β1, and hydroxyproline concentrations in the conditioned medium were decreased; STAT3 phosphorylation was significantly suppressed. Supplementation with Lv-IL-6 partially reversed these effects. The suppression of ISO-induced CF activation and fibrotic phenotype was associated with inhibition of IL-6 expression and blockade of IL-6/STAT3 signaling, suggesting the involvement of this pathway in the anti-fibrotic effects of BAZ. These findings provide in vitro evidence supporting BAZ as a candidate anti-myocardial fibrosis agent. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Approaches in Fibrosis and Tissue Remodeling)
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Review

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18 pages, 1802 KB  
Review
Proteinase-Activated Receptor 2 (PAR2) Deficiency and Cardiovascular Regulation: Context-Dependent Effects on Inflammation and Fibrosis
by Stephanie A. Viola, Shahnaz Siddiqua, Jesutofunmi Adesuyi, Yebin Jang, Maryia Ryskina and John J. McGuire
Curr. Issues Mol. Biol. 2026, 48(8), 821; https://doi.org/10.3390/cimb48080821 - 12 Aug 2026
Viewed by 442
Abstract
Proteinase-activated receptor 2 is a G protein-coupled receptor that regulates vascular tone and inflammatory signalling in the circulatory system. The roles of PAR2 appear complex and sometimes opposing. Studies using PAR2-deficient mice provide a framework to define these effects at the system level. [...] Read more.
Proteinase-activated receptor 2 is a G protein-coupled receptor that regulates vascular tone and inflammatory signalling in the circulatory system. The roles of PAR2 appear complex and sometimes opposing. Studies using PAR2-deficient mice provide a framework to define these effects at the system level. This review examines cardiovascular phenotypes associated with PAR2 deficiency in basal conditions and in disease. PAR2 deficiency produces modest increases in arterial blood pressure and vascular stiffness while preserving endothelial vasodilator function. Cardiac function remains largely normal in young PAR2-deficient animals but changes with age. Older PAR2-deficient mice develop diastolic dysfunction and cardiac fibrosis. In disease models, PAR2 deficiency has been associated with increased fibrosis in cardiac and vascular tissues and reduced vascular inflammation in atherosclerosis. PAR2 deficiency is also associated with reduced plaque progression and features of plaque stabilisation. In myocardial ischaemia models, PAR2 deficiency has been associated with reduced cardiac injury and adverse remodelling. The effects of PAR2 deficiency on inflammatory signalling vary according to tissue and disease context. Together, these findings suggest that the cardiovascular consequences of PAR2 deficiency depend on physiological and pathological context. Future studies should define cell-specific mechanisms to guide therapeutic targeting of PAR2. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Approaches in Fibrosis and Tissue Remodeling)
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